Evidence map›Paper›PMID 29697856›Full record

ArticleEuropean journal of immunology2018

Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment.

Jonathan J Grist, Brett S Marro, Dominic D Skinner, Amber R Syage, Colleen Worne, Daniel J Doty, Robert S Fujinami, Thomas E Lane

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 45 citations in OpenAlex.

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  15. Bioinformatic Analysis of the CXCR2 Ligands in Cancer Processes.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Jonathan J GristDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Brett S MarroDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.
Dominic D SkinnerDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Amber R SyageDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Colleen WorneDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Daniel J DotyDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Robert S FujinamiDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.
Thomas E LaneDepartment of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA.ORCID 0000-0003-0392-0825
University of Utah · USUniversity of California, Irvine · US

Funding

Chemokines and Viral-Induced Neurologic DiseaseR01NS041249 · NINDS · UNIVERSITY OF UTAH · PI LANE, THOMAS E · 2002 to 2019
$5.4M
Viral-induced axonopathy: mechanisms of damage and repairR01NS091939 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S, LANE, THOMAS E · 2016 to 2020
$1.7M
NINDS NIH HHS R01 NS041249NINDS NIH HHS R01 NS091939
6 · The paper itself

Abstract

Increasing evidence points to an important role for neutrophils in participating in the pathogenesis of the human demyelinating disease MS and the animal model EAE. Therefore, a better understanding of the signals controlling migration of neutrophils as well as evaluating the role of these cells in demyelination is important to define cellular components that contribute to disease in MS patients. In this study, we examined the functional role of the chemokine CXCL1 in contributing to neuroinflammation and demyelination in EAE. Using transgenic mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within glial fibrillary acidic protein-positive cells, we have shown that sustained CXCL1 expression within the CNS increased the severity of clinical and histologic disease that was independent of an increase in the frequency of encephalitogenic Th1 and Th17 cells. Rather, disease was associated with enhanced recruitment of CD11b

Indexed as

AnimalsAutoantigensCD11b AntigenCells, CulturedCentral Nervous SystemChemokine CXCL1Disease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalGene Expression RegulationHumansMiceMice, Inbred C57BLMice, TransgenicMolecular Targeted TherapyMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinAutoantigensCD11b AntigenChemokine CXCL1Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsAutoimmunityChemokinesDemyelinationNeuroinflammationNeutrophils

Identifiers

PMID29697856
PMCPMC6033633
OpenAlexW2802019846

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.